Wild Mustard (Sinapis arvensis) is a dicot weed in the Brassicaceae family. In Alberta this weed first evolved resistance to Group B/2 herbicides in 1993 and infests Canola, and Spring Barley. Group B/2 herbicides are known as ALS inhibitors (Inhibition of acetolactate synthase ALS (acetohydroxyacid synthase AHAS)). Research has shown that these particular biotypes are resistant to ethametsulfuron-methyl, and metsulfuron-methyl and they may be cross-resistant to other Group B/2 herbicides.

The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

Greenhouse trials comparing a known susceptible Wild Mustard biotype with this Wild Mustard biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on Group B/2 resistant Wild Mustard have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

Studies on the mechanism of resistance of Group B/2 resistant Wild Mustard from Alberta indicate that resistance is due to enhanced metabolism. There may be a note below or an article discussing the mechanism of resistance in the Fact Sheets and Other Literature

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of Group B/2 resistant Wild Mustard from Alberta please update the database.

The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Alberta have been instrumental in providing you this information. Particular thanks is given to Lyle Friesen, and John O'Donovan for providing detailed information.

The discovery of auxinic herbicides (e.g., 2,4-D, Dicamba, Picloram) for selective control of broad-leaf weeds in cereal crops revolutionized modern agriculture. These herbicides are inexpensive and do not generally have prolonged residual activity in soil. Although cultivated species of Brassicaceae (e.g., radish and other vegetables) are susceptible to auxinic herbicides, some biotypes of wild mustard (Sinapis arvensis, 2n=18) were found to be highly resistant to Picloram and Dicamba. Inter-generic hybrids between wild mustard and radish (Raphanus sativus, 2n=18) were produced by traditional breeding coupled with in vitro embryo rescue/ovule culture. To increase frequency of embryo regeneration and hybrid plant production, several hundred reciprocal crosses were performed between these species. Upon altering cultural conditions and media composition, a high frequency of embryo regeneration and hybrid plant establishment was achieved. A protocol was also optimized for in vitro clonal multiplication of inter-generic hybrids produced by embryo rescue. To evaluate transfer of auxinic herbicide resistance from wild mustard into hybrid plants, several screening tests (involving in vitro, molecular-based as well as whole plant-based tests) were performed. Results indicated that hybrids of R. sativus × S. arevensis were resistant to auxinic herbicides suggesting, that, the resistance trait was transferred to these hybrids from the wild mustard. This research for the first time demonstrates the possibility of transfer of auxinic herbicide resistance from wild mustard to radish..

BACKGROUND: Auxinic herbicides are widely used for selective control of many broadleaf weeds, e.g. wild mustard. An auxinic-herbicide-resistant wild mustard biotype may offer an excellent model system to elucidate the mechanism of action of these herbicides. Classical genetic analyses demonstrate that the wild mustard auxinic herbicide resistance is determined by a single dominant gene. Availability of near-isogenic lines (NILs) of wild mustard with auxinic herbicide resistance (R) and herbicide susceptibility (S) will help to study the fitness penalty as well as the precise characterization of this gene. RESULTS: Eight generations of backcrosses were performed, and homozygous auxinic-herbicide-resistant and auxinic-herbicide-susceptible NILs were identified from BC8F3 families. S plants produced significantly more biomass and seed compared with R plants, suggesting that wild mustard auxinic herbicide resistance may result in fitness reduction. It was also found that the serrated margin of the first true leaf was closely linked to auxinic herbicide resistance. Using the introgressed progeny, molecular markers linked to auxinic herbicide resistance were identified, and a genetic map was constructed. CONCLUSION: The fitness penalty associated with the auxinic herbicide resistance gene may explain the relatively slow occurrence and spread of auxinic-herbicide-resistant weeds. The detection of the closely linked markers should hasten the identification and characterization of this gene..

A greenhouse trial has been carried out with different herbicides to prove its efficiency on Sinapis arvensis population suspected to be resistant to tribenuron-methyl. The results confirm that this population survives to all rates of tribenuron-methyl treatments tested. However, this population can be controlled with other family of herbicides, such as 2, 4-D 60% and bromoxinil 12%+ioxinil 12%+mcpp-p 36%..